This Fellowship is awarded for a period of two years to an internationally established and already independent physician scientist, who will benefit from the opportunity to focus on research. The physician is integrated within the University Hospital Heidelberg and conducts her/his research in collaboration with an EMBL/MMPU group.
SCF awardee 2015:
Patrick Schweizer, MD, MSc
Patrick is physician for Cardiology in the Department of Cardiology, Angiology and Pulmonology, at the University Medical Center for Internal Medicine, Heidelberg
Residency and Research Associate at the Department of Cardiology, Angiology and Pulmonology, University Hospital Heidelberg, since 2004
2005 MD thesis, University of Heidelberg
2005-2007 Postdoctoral Research Fellowship at the Department of Cell Physiology, Max-Planck-Institute for Medical Research, Heidelberg, Germany
2009 Master (MSc) in Health Care Management, University of Mannheim
2012 Board certification “Internal Medicine”
HRCMM Senior Career Fellowship since 2015
Clinical host: Hugo A. Katus, Department of Cardiology, Angiology and Pulmonology, University Hospital Heidelberg
EMBL host: Rainer Pepperkok, Cell Biology and Biophysics
Disease studied: Cardiac arrhythmias
Sudden cardiac death as a result of malignant cardiac arrhythmias accounts for 15-20% of all-cause mortality. Currently, the management of patients with cardiac arrhythmias often is based on the implantation of electronic devices (pacemakers or defibrillators) to prevent fatal outcome, while causative therapies are not yet established. The voltage-gated sodium channel Nav1.5 underlies the depolarizing current INa, which is a key component for generation and propagation of the cardiac action potential. Loss of Nav1.5 function is associated with high arrhythmogenic risk in primary Mendelian rhythm disorders, as well as prevalent in heart failure and in acquired pathologies such as myocardial ischemia. Patrick aims to elucidate the mechanisms of sodium channel associated arrhythmias in vivo and at the molecular level using genetically altered mice and human samples. To do so he will study the molecular pathways that underlie maladaptive trafficking of Nav1.5 to the cell membrane leading to arrhythmias. It is the ultimate goal of this project to explore specific targets for the development of new antiarrhythmic strategies.
A Distinct Cardiomyopathy: HCN4 Syndrome Comprising Myocardial Noncompaction, Bradycardia, Mitral Valve Defects, and Aortic Dilation.
Schweizer PA, Koenen M, Katus HA, Thomas D.
J Am Coll Cardiol. 2017 Mar 7;69(9):1209-1210. doi: 10.1016/j.jacc.2016.10.085. PMID:28254188
TREK-1 (K2P2.1) K+ channels are suppressed in patients with atrial fibrillation and heart failure and provide therapeutic targets for rhythm control.
Lugenbiel P, Wenz F, Syren P, Geschwill P, Govorov K, Seyler C, Frank D, Schweizer PA, Franke J, Weis T, Bruehl C, Schmack B, Ruhparwar A, Karck M, Frey N, Katus HA, Thomas D.
Basic Res Cardiol. 2017 Jan;112(1):8. doi: 10.1007/s00395-016-0597-7. PMID: 28005193
Antiarrhythmic gene therapy - will biologics replace catheters, drugs and devices?
Lugenbiel P, Schweizer PA, Katus HA, Thomas D.
Eur J Pharmacol. 2016 Nov 15;791:264-273. doi: 10.1016 / j.ejphar.2016.09.001. Review.
Dilation of the Aorta Ascendens Forms Part of the Clinical Spectrum of HCN4 Mutations.
Vermeer AM, Lodder EM, Thomas D, Duijkers FA, Marcelis C, van Gorselen EO, Fortner P, Buss SJ, Mereles D, Katus HA, Wilde AA, Bezzina CR, Boekholdt SM, Schweizer PA, Christiaans I.
J Am Coll Cardiol. 2016 May 17;67(19):2313-5. doi: 10.1016/j.jacc.2016.01.086.